Factors influencing development of complications • Age • Poor socio-economic group • Virulence of organisms • Immune-compromised host • Preformed pathways • Cholesteatoma
Pathways of spread of Infection • Direct Bone Erosion • Venous Thrombophlebitis • Performed pathways
Classification • Intratemporal(confines within the temporal bone): • Mastoiditis • Petrositis • Facial paralysis • Labyrinthitis
B)Intracranial: • Extradural abscess. • Subdural abscess • Meninigitis • Brain abscess • Lateral sinus Thrombophlebitis • Otitic Hydrocephalus
1)Acute mastoiditis When the infection spreads from mucosal lining to bony wall of mastoid air cells we called it as mastoiditis. Aetiology: It usually accompanies or follows ASOM.The determining factors being high virulence of organisms or lowered resistance of patient.
Pathology: 1)Production of pus under tension. 2)Hyperaemic decalcification and osteoclastic resorption of bony walls.
Clinical Features: Symptoms: • Pain behind the ear. • Fever. • Ear discharge
Signs: • Mastoid Tenderness. • Ear Discharge • Sagging of postero-superior meatal wall • Perforation of tympanic membrane • Swelling over the mastoid • Hearing loss. • General findings
Investigations: • Blood counts • ESR • X-ray mastoid • Ear swab
Treatment: • Hospitalisation of patient • Antibiotics • Myringotomy • Cortical Mastoidectomy. It is indicated when there is • Sub-periosteal abscess. • Sagging of postero-superior meatal wall. • Positive resorvoir sign. • No response within 48 hrs of adequate medical treatment. • Mastoiditis leading to complications
2)Petrositis Spread of infection from middle ear and mastoid to petrous part of temporal bone is called petrositis. Clinical features: • Gradenigo’s syndrome : It is the classical presentation , and consist of a triad of a)external rectus palsy b)deep seated ear or retro orbital pain c)persistent ear discharge. • Fever , headache , vomiting , neck rigidity,facial paralysis.
Treatment: • Cortical , modified or radical mastoidectomy is often required. • Iv antibiotics should precede and follow surgical intervention.
3)Labyrinthitis: There are three types of labyrinthitis: a)Circumscribed labyrinthitis b)Diffuse serous labyrinthitis c)Diffuse suppurativelabyrinthitis
A)Circumscribed labyrinthitis(Fistula of labyrinth): There is thining or erosion of bony capsule of labyrinth. Aetiology: • CSOM with cholesteatoma • Neoplasms of middle ear • Surgical or accidental trauma to labyrinth
Clinical features: A part of membranous labyrinth is exposed and becomes sensitive to pressure changes . so complain of: • Triensient vertigo often induced by pressure on tragus, cleaning the ear or while performing valsalva manoeuvre. • Diagnose by fistula test. Treatment: a)Mastoid exploration. b)Systemic antibiotics.
B)Diffuse serous labyrinthitis It is diffuse intra-labyrinthine inflammation without pus formation and is a reversible condition if treated early. Aetiology: • Pre-existing circumscribed labyrinthitis associated with chronic middle ear suppuration or cholesteatoma. • In acute infections inflammation spreads through round window.
Clinical features: In mild cases-vertigo and nausea. In severe cases-vertigo is worse with marked nausea , vomiting and even spontaneous nystagmus. Chochlea is also affected with some degree of SNHL. Total loss of vestibular and cochlear function.
Treatment: Medical- • Bed rest • Antibacterial Therapy • Labyrinthine sedatives-prochlorperazine(stemetil) • Myringotomy if labyrinthitis has followed ASOM and drum is bulging. • Surgical: mastoidectomy
Diffuse suppurativelabyrinthitis: This is diffuse pyogenic infection of labyrinth with permanent loss of vestibular and cochlear functions. Aetiology: It usually follows serous labyrinthitis, pyogenic organisms entering through a fistula.
Clinical Features: • There is severe vertigo, nausea, and vomiting due to acute vestibular failure. • Spontaneous nystagmus. • Patient looks toxic with total loss of hearing. Treatment:
B)Intracranial complications : Otogenic brain abscess: 50% of brain abscess in adults and 25%in children are otogenic .Cerebral abscess is seen twice as frequently as cerebellar abscess. Routes of infection: They develops as a result of direct extension of middle ear infection through tegmen or by thrombophlebitis.
Pathology: a)Stage of invasion(initial encephalitis) b)Stage of localisation(latent abscess) c)Stage of enlargement(manifest abscess) d)Stage of termination(rupture of abscess)
Clinical Features: Brain abscess is often associated with other complications. It can be divided into: a)Those due to raised ICP b)Those due to area of brain affected
a)Symptoms and sign of raised ICP • Headache • Nausea and vomiting • Level of consciousness • Papiloedema • Slow pulse and subnormal temp.
b)Localising Features: Temporal lobe abscess: • Nominal Aphasia • Homonymous hemianopia • Contralateral motor paralysis • Epeliptic fits
Investigations: a)Skull x-rays including mastoids b)CT scan c) LP Treatment: • High dose of iv antibiotics. • For raised ICP-Dexamethasone 4mg iv 6 hrly • Discharge from ear is treated by suction clearance and topical ear drops. • Neurosurgical treatment.
LATERAL SINUS THROMBOPHELEBITIS • ETIOLOGY: • COMPLICATION OF ACUTE COALESCENT MASTOIDITIS,MASKED MASTOIDITIS OR CHRONIC SUPPURATION OF MIDDLE EAR AND CHOLESTEATOMA • CLINICAL FEATURE • HETIC TYPE OF FEVER WITH RIGOR • HEADACHE • PROGRESSIVE ANAEMIA &EMACIATION • PAPILLOEDEMA
TRETMENT • SYSTEMIC ANTIBACTERIAL • MASTOIDECTOMY & EXPOSURE OF SINUS • LIGATION OF INTERNAL JUGULAR VEIN • ANTICOAGULANT THERAPY • SUPPORTIVE TRETMENT